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β-Cells at the Center of Type 1 and Type 2...
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β-Cells at the Center of Type 1 and Type 2 Diabetes

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2813

Special Issue Editor

Dr. Jeffery S. Tessem

E-Mail Website
Guest Editor
Nutrition, Dietetics and Food Science Department, Brigham Young University, Provo, UT 84602, USA
Interests: beta cell; insulin secretion; cell cycle; mitochondrial respiration;nuclear hormone receptors; Nr4a1; Nr4a3

Special Issue Information

Dear Colleagues, 

Damage to and the failure of pancreatic beta cells are central to type 1 and type 2 diabetes. Impaired insulin secretion, insufficient proliferation, increased cell death, and dedifferentiation lead to impaired functional beta cell mass, which is central to T1D and T2D disease progression. Our understanding of the mechanisms and function of the beta cell under healthy and diseased conditions, as well as across the life cycle, has greatly expanded. Studies focusing on function, survival, replication, structure, epigenetics, and “omics” data have begun to help us understand the central role that the beta cell has in T1D and T2D. This Special Issue aims to highlight the changes to the beta cell across both T1D and T2D, as well as throughout the lifespan. In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: beta cell mass, beta cell function, beta cell signaling, beta cell death, beta cell ER stress, glucolipotoxicity and the beta cell, and beta cell dedifferention.

We look forward to receiving your contributions.

Dr. Jeffery S. Tessem
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • beta cell
  • insulin secretion
  • cell cycle
  • mitochondrial respiration
  • nuclear hormone receptors
  • Nr4a1
  • Nr4a3

Published Papers (2 papers)

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Research

15 pages, 3378 KiB  
Article
CEBPA Overexpression Enhances β-Cell Proliferation and Survival
by Peter N. Ellsworth, Jacob A. Herring, Aaron H. Leifer, Jason D. Ray, Weston S. Elison, Peter Daniel Poulson, Jacqueline E. Crabtree, Pam M. Van Ry and Jeffery S. Tessem
Biology 2024, 13(2), 110; https://doi.org/10.3390/biology13020110 - 09 Feb 2024
Viewed by 1327
Abstract
A commonality between type 1 and type 2 diabetes is the decline in functional β-cell mass. The transcription factor Nkx6.1 regulates β-cell development and is integral for proper β-cell function. We have previously demonstrated that Nkx6.1 depends on c-Fos mediated upregulation and the [...] Read more.
A commonality between type 1 and type 2 diabetes is the decline in functional β-cell mass. The transcription factor Nkx6.1 regulates β-cell development and is integral for proper β-cell function. We have previously demonstrated that Nkx6.1 depends on c-Fos mediated upregulation and the nuclear hormone receptors Nr4a1 and Nr4a3 to increase β-cell insulin secretion, survival, and replication. Here, we demonstrate that Nkx6.1 overexpression results in upregulation of the bZip transcription factor CEBPA and that CEBPA expression is independent of c-Fos regulation. In turn, CEBPA overexpression is sufficient to enhance INS-1 832/13 β-cell and primary rat islet proliferation. CEBPA overexpression also increases the survival of β-cells treated with thapsigargin. We demonstrate that increased survival in response to ER stress corresponds with changes in expression of various genes involved in the unfolded protein response, including decreased Ire1a expression. These data show that CEBPA is sufficient to enhance functional β-cell mass by increasing β-cell proliferation and modulating the unfolded protein response. Full article
(This article belongs to the Special Issue β-Cells at the Center of Type 1 and Type 2 Diabetes)
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15 pages, 2212 KiB  
Article
Toll-like Receptor 9 Gene in the Development of Type 2 Diabetes Mellitus in the Saudi Arabian Population
by Zeina S. Alkudmani, Aminah Ahmad Alzailai, Khaled H. Aburisheh, Amal F. Alshammary and Imran Ali Khan
Biology 2023, 12(11), 1439; https://doi.org/10.3390/biology12111439 - 16 Nov 2023
Cited by 1 | Viewed by 1079
Abstract
Diabetes mellitus is a complex disease with a wide range of manifestations. Diabetes, notably type 2 diabetes mellitus (T2DM), is becoming more common in Saudi Arabia as a result of obesity and an aging population. T2DM is classified as a noncommunicable disease, and [...] Read more.
Diabetes mellitus is a complex disease with a wide range of manifestations. Diabetes, notably type 2 diabetes mellitus (T2DM), is becoming more common in Saudi Arabia as a result of obesity and an aging population. T2DM is classified as a noncommunicable disease, and its incidence in the Saudi population continues to grow as a consequence of socioeconomic changes. Toll-like receptors (TLRs) are innate immune receptors that mediate the inflammatory response in diabetes mellitus. Previous studies have documented the relationship between different SNPs in the TLR9 gene in different forms of diabetes. As a result, the purpose of this study was to investigate the relationship between rs187084, rs352140, and rs5743836 SNPs in the TLR9 gene among T2DM patients in the Saudi population. This was a case-control study that included 100 T2DM cases and 100 control subjects. The three SNPs were identified in the study population (n = 200) using polymerase chain reaction (PCR), restriction enzymes for rs352140, and Sanger sequencing for rs187084 and rs5783836. Next, statistical analyses were performed using various software to determine the association between the SNPs and T2DM. rs187084 and rs5743836 were associated with an increased risk of T2DM development. rs187084 and rs5743836 allelic frequencies were associated with a 3.2 times increased risk of T2DM development (p < 0.05). DBP was associated with T2DM (p = 0.02). rs187084 was associated with TC and HDLc; rs352140 was associated with DBP, HbA1c, and HDLc; rs5743836 was associated with waist (p < 0.05). The CGT haplotype was strongly associated with T2DM (p < 0.003). Gene–gene interaction, graphical presentation, and dendrogram showed the strong association with T2DM patients (p < 0.05). This study concluded that rs187084 and rs5743836 were strongly associated with T2DM in Saudi Arabian patients. This study provides further evidence that SNPs in the TLR9 gene play a significant role in T2DM development in a Saudi community. Full article
(This article belongs to the Special Issue β-Cells at the Center of Type 1 and Type 2 Diabetes)
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